Oncological Emergencies Flashcards

1
Q

What is tumour lysis syndrome?

A

Rapid destruction of cancer cells after chemo or spontaneously which leads to intra cellular contents being released into the blood stream.

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2
Q

What does tumour lysis syndrome lead to.

A

An elevation in serum uric acid, K+, phosphate, and a reduction in serum Ca2+ levels.

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3
Q

Which patients are at a particular risk of having tumour lysis syndrome?

A
. High tumour burden 
. Rapidly proliferating tumour 
. Haematological disease
. Bulky disease
. Pre existing renal impairment 
. Hypovolaemia 
. Diuretic use pre treatment 
. High levels of LDH/ uric acid in the serum pre treatment
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4
Q

What do you need to diagnose tumour lysis syndrome?

A

1 clinical feature + 2 lab features….

Clinical features...
. An increased serum creatinine 
. Cardiac arrythmia 
. Seizure 
. Sudden death 
2 lab features...
. Increased uric acid 
. Increased K+ 
. Increased phosphate 
. Decreased Ca2+
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5
Q

How can you help prevent tumour lysis syndrome?

A

Hydration is key before and after chemo to stop uric acid from accumulating
Patients at risk of TLS should be given allopurinol or Rasburicase

(These are medications that help clear uric acid from the blood)

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6
Q

How does rasburicase work?

A

Converts uric acid to allantoin which is much more water soluble and therefore more gets excreted in the kidney.

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7
Q

How does allopurinol work?

A

Xanthine oxidase inhibitor which lowers the uric acid levels

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8
Q

Should you ever give rasburicase and allopurinol together?

A

Never, allopurinol reduces the affect of rasburicase.

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9
Q

How can you lower uric acid levels if rasburicase and allopurinol don’t work, if refractory or severely raised?

A

Dialysis can be used

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10
Q

What is the risk of tumour lysis syndrome?

A

AKI and permanent renal damage

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11
Q

How do you manage tumour lysis syndrome?

A

Fluids!!!!
IV rasburicase +/- dialysis (for severe renal impairement)

10ml IV calcium gluconate 10% for symptomatic hypocalcaemia

Insulin and dextrose

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12
Q

What is neutropenic sepsis?

A

A severe widespread response to an infection which is greatly exaggerated due to the low levels of neutrophils in a patient undergoing chemo.

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13
Q

When does neutropenic sepsis usually occur?

A

5-14 days after chemo when neutrophils are at the lowest.

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14
Q

What are the usual causative organisms of neutropenic sepsis?

A

Usually endogenous flora- staph aureus

Although a lot of the time no causative organisms are found.

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15
Q

What patients are at risk of neutropenic sepsis?

A

Inpatients
Those with severe/prolonged neutropaenia
Those with significant co morbidities like COPD/ diabetes
Those with central lines/mucosal disruption

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16
Q

How is neutropenic sepsis diagnosed?

A

Bloods- FBC, U and Es, LFTs, blood cultures, CRP, lactate
Sepsis 6
CXR
Urine, stool, sputum if clinically indicated
Central and peripheral line swabs
Swabs of catheters/ indwelling lines

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17
Q

When is a diagnosis of neutropenic sepsis made?

A

Neutrophil count <0.5x10^9
They have been receiving systemic anticancer therapy
They have a temp >38 or other signs of sepsis

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18
Q

How do you manage neutropenic sepsis?

A

Broad spec abx with IV tazocin or meropenem

Fluid resuscitation and fluid balance

G-CSF can be given to boost the patients immune system (artificial neutrophils)

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19
Q

How can you prevent neutropenic sepsis from occuring?

A

Prophylactic abx- fluoroquinolone
Patients should carry around a yellow alert card
Patients should be made aware of warning signs
24 hour contact number for help if they notice signs of infection

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20
Q

Beyond what level is spinal cord compression classed as cauda equina?

A

Below the level of L2

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21
Q

What is the NICE definition of neutropenic sepsis?

A

Patient undergoing systemic anti cancer treatment (SACT)

Temp >38

Neutrophil count <0.5 x 10^9 per litre

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22
Q

When does neutropaenia typically occur after chemo?

A

Typically occurs day 10-14

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23
Q

What are the signs and symptoms of neutropenic sepsis?

A

Fever
Symptoms related to a specific system- cough, SOB
Drowsy
Confused

Signs 
Febrile 
Tachy >90 
Hypotension <90 systolic- needs urgent attention 
RR >20 
Impaired MMSE
Signs of infection
24
Q

What are the most common pathogens which cause neutropaenic sepsis?

A

80% arise from endogenous flora (due to disruption of mucosal lining)

Increasing frequency of gram +ve cocci; indwelling plastic catheters promote colonisation

Most frequent isolates= staph aureus, staph epidermidis, enterococcus and streptococcus

MRSA and VRE are increasingly prevalent

Source identified in approximately 30% of patients

25
Q

What investigations are done for someone with neutropaenic sepsis?

A
Blood tests: 
FBC (with differential) 
U and Es 
LFTS 
Lactate 
CRP 
ABG 

Cultures
Blood- central and peripheral
Urine
sputum

Swabs
Lines
Wounds

Imaging
Directed clinically
CXR, AXR, CT/MRI

26
Q

What is the differential diagnosis for neutropaenic sepsis?

A

Malignant related fever
PE
Chemo related fever

27
Q

What is the management of neutropaenic sepsis?

A
Dont wait for the FBC
Empiric IV broad spec within the hour (meropenem or 
Fluid rescucitation 
Consider catheterisation 
Involve senior members of rhe ream 
Consider the need for escalation of care
28
Q

What can be considered in patients who are profoundly septic/neutropenic where you have already done the above management?

A

GCSF (granulocyte colony stimulating factor)

29
Q

How can you avoid neutropaenic sepsis?

A

Patient education- how and when to contact 24 hour specialist oncology advice/ seek emergency care

Antibiotic prophylaxis (versus increased antibiotic resistance)

Dose reduction (palliative chemo), prophylactic GCSF (curative/ adjuvant) should be Considered for future chemo cycles

All patients should be issues with an alert card with 24 hour contact numbers

30
Q

What cancers are most likely to metastasise to the spine?

A

Breast, lung, prostate

31
Q

At what level does cauda equina occur?

A

Below L2, cauda equina is the compression of peripheral nerves not the spinal cord

32
Q

What is the pathophysiology behind metastatic spinal cord compression?

A

Usually caused by collapse or compression of a vertebral body that contains metastatic disease (arterial seeding)

10% by direct tumour (paraspinal mass) extension into the vertebral column

Compression of the cord initially causes oedema, venous congestion and demyelination which are reversible

Prolonged compression leads to vascular injury, cord necrosis and permanent damage

33
Q

How does MSCC present?

A

> 90% have back pain
Back pain is frequently the first symptom and prolonged; often precedes other symptoms by 2-3/12
Spinal or radicular pain (8/10)
Exacerbated by straight leg raising, coughing, sneezing, straining

> 75% have limb weakness
50% have sensory level (not cauda equina)
40% have bladder and anal sphincter dysfunction
Diminishing performance status/generally unwell

34
Q

What presentation would someone have on examination with spinal cord compression due to mets?

A

Acute onset of flaccid paralysis

Progressing over time.,,

Spasticity (increased tone, clonus, hyperreflexia in limbs) below the level of metastatic spinal cord compression

Plantar reflexes would be up going (but not with cauda equina)

Sensory loss with a well defined dermatonal level

Palpable bladder (urinary retention)

35
Q

What should you do if you suspect MCSS?

A
MRI within 24 hours 
Admit 
Bed rest with log rolling 
Dexamethasone 16mg + PPI 
Adequate analgesia 
Treatment within 24 hours of diagnosis
36
Q

What is the treatment of MSCC?

A

The treatment of choice is surgery if fit and good prognosis (>3/12)

Multiple myeloma, lymphoma, breast, prostate, renal cancers

Good motor function at presentation, good performance status, limited comorbidity, single level spinal disease, absence of visceral mets, long interval from primary diagnosis, also for biopsy or stabilisation

37
Q

What does the surgery do?

A

Relieves compression

Removes tumour and stabilises spine

38
Q

What other options other than surgery do you have for MCSCC?

A

Balloon kyphoplasty
Radiotherapy (this is what is used for the majority with extensive disease and poor physiological reserve), it should be delivered within 24 hours of confirmation

39
Q

How does radiotherapy work for MCSCC?

A

It relieves compression of the spine and nerve roots by causing cell death in the rapidly dividing tumour tissue.

40
Q

What are the supportive care options for MCSCC?

A
Good nursing care, 
Analgesia 
Laxatives 
Bladder care 
Monitor BMs 
VTE prophylaxis 
Physiotherapy 
Occupational therapy 
Urgent chemo for sensitive tumours- lymphoma, teratoma, SCLC
41
Q

What is the median survival of people with MSCC?

A

Those who do not recover their mobility: 1-3/12
If they can walk: 5-8/12
Patients with myeloma/lymphoma have an even longer prognosis

42
Q

What is the normal calcium range?

A

2.2-2.6mmol/L (corrected)

43
Q

What is hypercalcaemia most common in?

A

Most common in squamous cell cancers (lung, H and N, kidney, cervix).

44
Q

What is hypercalcaemia usually caused by in terms of cancerz?

A

Generally due to a paraneoplastic phenomenon (tumour secretion PTH related peptide)
This leads to…
Increased bone resorption and renal reabsorption
Unrelated to the extent of bone mets
(80%)

Other causes…

Osteolytic metastases with local release of cytokines (20%), causes increased bone resorption and calcium release from bone (local bone destruction)

Tumour production of 1,25 dihydroxy vitamin D (lymphoma) leads to increased intestinal calcium absorption and bone resorption

45
Q

What are the symptoms of hypercalcaemia in the cancer patient?

A
Often non specific; the severity relates to the rate of increase 
Nauseated 
Anorexia 
Thirsty 
Polydipsia and polyuria 
Fatigue and weakness 
Constipated 
Confused 
Poor concentration 
Drowsy 
Severe N&V, ileus, delirium, coma and death
46
Q

How do you treat hyprcalcaemia?

A

FLUIDS!! Rehydration is so important, there should be at least 24 hours of normal saline.

Bisphosphonates
60-90mg pamidronate IV or IV zolendronic acid 4mg
Bisphosphonates can cause renal failure therefore you should make sure the patient is properly rehydrated first
Bisphosphonates can take up to a week to work

47
Q

How do you treat hypercalcaemia that is refractory to zoledronic acid/ bisphosphonates are contraindicated in?

A

Denosumab

48
Q

What is tumour lysis syndrome?

A
Massive tumour cell lysis which leads to the release of large amounts of K+, phosphate and uric acid into the systemic circulation 
Leads to...
Hyperuricaemia 
Hyperkalaemia 
Hyperphosphataemia 
AKI 
Hypocalcaemia
49
Q

What are the susceptible tumour types for tumour lysis syndrome?

A

The risk is greatest for haematological malignancies
Bulky chemo responsive tumours
Most common with high grade lymphomas and leukaemias

It is generally following the initiation of cytotoxic therapy

50
Q

What are the patient specific risk factors for tumour lysis syndrome?

A

Pre existing renal dysfunction/nephropathy
Pre treatment hyperuricaemia
Hypovolaemia (pre treatment diuretic use)
Pre treatment high LDH
Urinary tract obstruction from tumour

51
Q

What is the presentation of tumour lysis syndrome?

A
This is normally 3-7 day post chemo 
Nausea and vomiting 
Diarrhoea 
Anorexia 
Lethargy 
Haematuria -> oliguria -> anuric 
Heart failure
Cardiac arrythmias/arrest (peaked T waves, QTc derangement) 
Primary presentation of malignancy= ‘spontaneous tumour lysis’
52
Q

How do you prevent/treat tumour lysis syndrome?

A

Pre hydration and vigorous hydration throughout treatment
Monitoring of electrolytes and fluid balance
Allopurinol
Rasburicase

53
Q

What is SVCO?

A

Obstruction of blood flow through the SVC
Compression or occlusion of SVC
90% are usually extrinsic compression- intrathoracic primary, lung cancer (80%), mesothelioma

Can occasionally get a benign obstruction- thrombus

Uncommon causes= post RT fibrosis, TB

54
Q

What are the signs and symptoms of SVC obstruction?

A
Breathlessness (50%) 
Swelling of the face and neck (40%) 
Trunk and arm swelling (40%) 
Sensation of choking 
A feeling of fullness in the head 
Headache 
Lethargy 
Chest pain 
Cough dysphagia 
Cognitive dysfunction 
Hallucinations 
Seizures
Stridor 
Coma
55
Q

How do you investigate SVCO?

A

CT with contrast

56
Q

What is the treatment of SVCO?

A

Steroids (frequently prescribed, however there is no evidence to support their use)

Stent: if not radio or chemo sensitive
95% desponse rate
Rapid relief of symptoms, but doesnt actually treat the cause

Chemo used for SCLC, lymphoma, teratoma (response rate >70%)

Radiotherapy- used for other malignant causes